Qoronfleh M W, Gustafson J E, Wilkinson B J
Department of Biological Sciences, Illinois State University, Normal 61790-4120, USA.
FEMS Microbiol Lett. 1998 Sep 1;166(1):103-7. doi: 10.1111/j.1574-6968.1998.tb13189.x.
When Staphylococcus aureus strain 8325 was grown at 30 degrees C and heat shocked at 40 degrees C the rate of cell autolysis in buffer with or without Triton X-100 was reduced. Treatment of growing cells with other agents (CdCl2, ethanol, NaCl) known to induce heat shock proteins also resulted in cells that showed a decreased rate of autolysis. Heat shocked cells showed lower rates of freeze-thaw autolysin activity on purified cell walls, and isolated crude cell walls from heat shocked cells had lower rates of autolytic activity compared to controls. No differences in the peptidoglycan hydrolase activity profiles of control and heat shocked cells were detected by renaturing sodium dodecyl sulfate polyacrylamide gel electrophoresis. It is proposed that autolysins are damaged by heat shock and their targeting to the cell wall is impaired, possibly by complexing with heat shock proteins, which may also inhibit autolysin activity. Heat shock also inhibited the autolytic activity of methicillin-resistant and related-susceptible strains, and the possible relationship of this to the expression of methicillin resistance is discussed.
当金黄色葡萄球菌8325菌株在30℃下生长并在40℃下进行热激处理时，无论有无Triton X-100，其在缓冲液中的细胞自溶速率均降低。用已知可诱导热休克蛋白的其他试剂（CdCl2、乙醇、NaCl）处理生长中的细胞，也会导致细胞自溶速率降低。热激处理的细胞在纯化细胞壁上的冻融自溶素活性较低，并且与对照相比，从热激处理的细胞中分离出的粗细胞壁的自溶活性较低。通过复性十二烷基硫酸钠聚丙烯酰胺凝胶电泳未检测到对照细胞和热激处理细胞的肽聚糖水解酶活性谱有差异。有人提出，自溶素因热激而受损，其靶向细胞壁的能力受损，可能是由于与热休克蛋白结合，这也可能抑制自溶素活性。热激还抑制了耐甲氧西林菌株和相关敏感菌株的自溶活性，并讨论了这与耐甲氧西林表达的可能关系。
